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Hepatocystin is Essential for TRPM7 Function During Early Embryogenesis.

Jeffrey D Overton1, Yuko Komiya1, Courtney Mezzacappa2

  • 1Rutgers-Robert Wood Johnson Medical School, Dept. of Pharmacology, Piscataway, 08854, USA.

Scientific Reports
|December 17, 2015
PubMed
Summary

Hepatocystin (PRKCSH) loss impairs TRPM7 expression, crucial for gastrulation. Overexpressing TRPM7 rescues developmental defects, revealing TRPM7

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Area of Science:

  • Developmental Biology
  • Molecular Genetics
  • Cell Biology

Background:

  • Mutations in PRKCSH cause polycystic liver disease (PCLD).
  • Hepatocystin (80K-H) is the beta subunit of Glucosidase II, involved in glycoprotein processing.
  • PRKCSH mutations are linked to renal cysts via PKD2 interference.

Purpose of the Study:

  • Investigate hepatocystin function in Xenopus laevis embryogenesis.
  • Identify hepatocystin's role in vertebrate gastrulation.
  • Determine the molecular mechanism underlying hepatocystin-related embryonic lethality.

Main Methods:

  • Studied hepatocystin function during Xenopus laevis embryogenesis.
  • Identified hepatocystin as a binding partner of the TRPM7 ion channel.
  • Assessed the effects of TRPM7 overexpression and hepatocystin depletion on gastrulation.

Main Results:

  • Hepatocystin interacts with TRPM7, essential for gastrulation.
  • TRPM7 overexpression rescued gastrulation defects in hepatocystin-deficient embryos.
  • Hepatocystin depletion reduced TRPM7 expression in Xenopus embryos.

Conclusions:

  • Hepatocystin and TRPM7 function synergistically during gastrulation.
  • Embryonic lethality from hepatocystin loss is primarily due to impaired TRPM7 expression.
  • Hepatocystin's role in early development is significantly mediated by its interaction with TRPM7.